Selenate and maximum lifespan in rats.
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timoth ...@my-deja.com (Tim)
I recall this study showed an increase in maximum lifespan in rats with sodium selenate. The Journal of Nutrition's online archives don't go back that far. I have a secondary source of the results of the study somewhere if I can find it. Perhaps someone has ready access to this paper.
Shroeder HA ,Mitchener M. Selenium and tellurium in rats: effect on growth, survival and tumors. J Nutr 1971 Nov, 101(11):1531-40 PMID: 5124041 http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&... (From LEF Website) Selenium There has never been a study to test the effects on lifespan of the trace mineral selenium, but an early study, which examined the toxicity of selenium (and other minerals) found, by accident, that it extended the lifespan of laboratory mice. Anyone taking selenium on a daily basis for antiaging purpose should be careful to keep their doses low to avoid the possibility of toxic side effects.
Tim
timoth ...@my-deja.com (Tim)
Doug Skrecky reports the results as follows.
The greatest maximum life span was 46.6 months for one of two control groups from reference 10. However the maximum life span for some of the treated groups was even longer. The treated groups with the greatest maximum life spans are as follows: REF INTERVENTION MAXIMUM AVERAGE 4 selenate 2 ppm 61 months 33.8 months 10 sodium arsenite 5 mg/l & chromium 1 mg/l 53.2 27.5 6 -70 tryptophan 50.9 6.7 2 beryllium 5 ppm 48.8 29.7 14 -24% chow & exercise 48.1 33.2 1 chromium picolinate 1 mg/kg 48 44 10 control group 46.6 31.5 http://www.cryonet.org/cgi-bin/dsp.cgi?msg=8666 Tim
"michaelprice" michaelpr...@ntlworld.com
Thanks Tim, That's interesting: Doug seems to be saying that selenate increased the maximum lifespan of rats, but not much effect in the average LS, whereas Walford (who gives the same reference[2]) says the average LS was increased, but *not* the maximum LS. Walford in the past, I have not found to be a reliable reporter of such things, but the graph shown in his book (page 389, the 120 yr diet) seems to bear out his ***ertion.
A trip to the library is in order, methinks.
Selenate 2ppm? Is that by weight in the water? If it is then a human equivalent would be (***uming 1 litre of water/d) 2mg?
Walford also mentions another interesting reference which showed that selenium delayed the onset of tumours, which he took (unusually!) as indicating that perhaps the aging process had been slowed down: Ann Clin Lab Sci. 1974 Nov-Dec;4(6):441-7.
Effects of selenium and of arsenic on the genesis of spontaneous mammary tumors in inbred C3H mice.
Schrauzer GN, Ishmael D.
PMID: 4473954 1: Schroeder HA, Mitchener M.
Selenium and tellurium in mice. Effects on growth, survival, and tumors.
Arch Environ Health. 1972 Jan;24(1):66-71. No abstract available.
PMID: 4500615 2: Schroeder HA, Mitchener M.
Selenium and tellurium in rats: effect on growth, survival and tumors.
J Nutr. 1971 Nov;101(11):1531-40. No abstract available.
PMID: 5124041 3: Schroeder HA, Mitchener M.
Toxic effects of trace elements on the reproduction of mice and rats.
Arch Environ Health. 1971 Aug;23(2):102-6. No abstract available.
PMID: 5558140 Cheers, Michael C Price
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timoth ...@my-deja.com (Tim)
I was hoping Doug would reply he seems to have the paper.
I have a paper on this if I can find I will post.
Regards, Tim
"JG" nos...@maol.com
Yes, 2 ppm in water. Since average water consumption in a rat is 35 mL/d this is about 70 mcg/d--quite a high consumption (no wonder selenite was so toxic in this study). The human equivalent would be something like 3 mg/d if you scaled by calories or diet.
timoth ...@my-deja.com (Tim)
Selenite would appear to be a poor choice due to toxicity and poor bioavailibility. Yeast appears to be the preferred form far less toxic and absorbed by the tissues better. So it may be more effective at far lower doses.
It also increased GSHPx activity 163%.
SelenoSource AF is more bioavailable. Table 1: Selenium relative recovery (%) Sodium Selenite SelenoSource AF Serum 100 200 GSHPx Activity 100 163 Liver 100 206 Breast Muscle 100 1280 Sims, M.D., Virginia Scientific Research Inc., 2001.
In a recently conducted study with 800 commercial broiler chickens (Table 1), the relative recovery of SelenoSource AF was ***essed per kg of body weight. This study established that the amount of selenium available from SelenoSource AF should be an integral part of feeding programs, especially those where stress and maximum production are critical.
The Importance of Bioavailability.
Other research work has also shown that organic selenium is more bioavailable than inorganic selenium. In addition, selenium concentrations as well as glutathione peroxidase (GSHPx) activity are maintained for a longer period after supplementation with organic selenium. Hence, organic selenium when fed is in a "ready to use" form and can be incorporated into functional selenoproteins required by the body without reduction and methylation to selenides as is the case with sodium selenate or selenite.
In addition, inorganic selenium does not contribute to the storage pool i.e., cannot be stored in muscles, colostrums and milk protein, egg white and egg yolk. Consequently, the antioxidant defense system and immunity during stress, parturition, neonatal and embryonic stage is compromised when inorganic selenium is used. This explains why SelenoSource AF is recommended to improve reproductive performance, embryonic and neonatal survival, stress resistance and increase growth rates, egg and muscle quality (reduced drip loss).
http://www.diamondv.com/products/selenosource_af/availibility.htm Tim
"michaelprice" michaelpr...@ntlworld.com
Thanks Tim and JG.
I said: Upon looking up the articles I see that the claim that Walford makes, that selenate does not extend maximum lifespan, turns out to be another example of his biased and skewed reporting against supplements.
Yes, the graph he reproduces to support his claim was copied from [2], but he fails to mention that the longest lived survivor was not portrayed on the graph. As JG reported of the original article: Was the 5yr lifespan of the selenate-fed rat a statistical fluke?
In the other study [1] on mice the same thing was observed, viz a very long-lived survivor in the selenate group, but not in the control group, so the possibility of a fluke is looking less likely. I'm upgrading the importance of selenium in my regime.
1: Schroeder HA, Mitchener M.
Selenium and tellurium in mice. Effects on growth, survival, and tumors. Arch Environ Health. 1972 Jan;24(1):66-71.
PMID: 4500615 2: Schroeder HA, Mitchener M.
Selenium and tellurium in rats: effect on growth, survival and tumors. J Nutr. 1971 Nov;101(11):1531-40.
PMID: 5124041 Cheers, Michael C Price
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"michaelprice" michaelpr...@ntlworld.com
Follow-up on the Schroeder et al experiments [1,2] on rodents with selenium and tellurium.
Tellurium lies directly below selenium in the periodic table, sharing many of its properties. Tellurium (along with selenium, as previously reported) extended the maximum lifespan of the test animals, relative to the controls. This means that of the four test groups, three had their maximum lifespans extended, and extended by a great deal. These can't easily be dismissed as statistical flukes, since there were three control groups (one for the comparison with selenate fed rats and two for the mice). Typically maximum lifespans do not reach twice the average lifespan (e.g. 70+ vs 123 for humans), whereas here we see (maximum treated LS / mean control average LS) of between 2.25 to 2.62, giving a human-equivalent maximum lifespan of 180+ years.
The problem with selenium, from a life-extensionist POV is that the mean LS was not raised by even 20% in any of the test groups, whereas other putative anti-aging supplements extend the mean lifespan by more than the maximum lifespan.
I interpret this as meaning that putative anti-aging supplements normally improve health as well as slowing down aging. In the above experiments the selenium or tellurium seemed to slow aging (extend maximum LS) but *worsen* health (poor avg LS).
However I think this is easily "explainable": the dose used was toxic which was why, in the rats in particular, the number of age-adjusted malignant tumours was increased (by selenium given as selenate) from 17% to 42%. The maximum lifespan extensions were exhibited by a subset of the rodents able to tolerate the high doses of selenium or tellurium.
The question remains whether we would see a similar increase in mean lifespan, as found for maximum lifespan, if a lower, non-
toxic dose of selenium (or tellurium) were used.
1: Schroeder HA, Mitchener M.
Selenium and tellurium in mice. Effects on growth, survival, and tumors. Arch Environ Health. 1972 Jan;24(1):66-71.
PMID: 4500615 2: Schroeder HA, Mitchener M.
Selenium and tellurium in rats: effect on growth, survival and tumors. J Nutr. 1971 Nov;101(11):1531-40.
PMID: 5124041 (I've ignored the effects of selenite (as opposed to selenate) on rats, which was highly toxic.) Cheers, Michael C Price
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Tim Tyler t...@tt1lock.org
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Tim Tyler t...@tt1lock.org
[Sincere apologies for the previous post without any commentary] michaelprice <michaelpr...@ntlworld.com> wrote or quoted: [...] I think the "selenium hormesis" hypothesis deserves more attention.
Ignore for a moment the fact that selenium plays a role in some anti-oxidant enzymes - and consider the fact that it is a potent apoptosis inducer, inhibits growth and cell division - and is basically a toxic agent.
What I think is going on is that the body's defense mechanisms are being activated by the toxic ***ault. This up-regulates the body's healing and repair mechanisms - and probably down-regulates everything else.
The following seems to suggest the "anti-cancer" response to selenium takes the form of a stress response: ``Based on the above information, it is proposed that the mitochondrial pathway and the endoplasmic reticulum stress/cytokine signaling pathway might be involved in apoptosis induction by VES and [methylseleninic acid (MSA), a selenium metabolite], respectively.'' ``Synergy between selenium and vitamin E in apoptosis induction is ***ociated with activation of distinctive initiator caspases in human prostate cancer cells'' - http://calorierestriction.org/pmid/?n=14583501 This suggests selenium's activity in terms of preventing DNA damage does /not/ depend on the activity of glutathione peroxidase: ``The extent of DNA damage in prostate cells and in peripheral blood lymphocytes, as determined by the alkaline comet ***ay, was lower among the selenium-supplemented dogs than among the control dogs (prostate P<.001; peripheral blood lymphocytes P =.003; analysis of variance) but was not ***ociated with the activity of the antioxidant enzyme glutathione peroxidase in plasma.'' ``Effects of dietary selenium supplementation on DNA damage and apoptosis in canine prostate.'' - http://calorierestriction.org/pmid/?n=12569146 The idea of selenium hormesis certainly helps explain why maximum lifespan was affected more than everage lifespan - hormetic stress responses are /only/ theraputic /if/ you can handle them.
The effect of tellurium is explained in the same way: tellurium is /also/ a toxic substance: ``Although rarely encountered except in industrial settings, tellurium is relatively toxic, with acute exposure causing a variety of gastrointestinal and neurological symptoms, and death in severe exposures.'' - http://www.uky.edu/Pharmacy/ps/porter/Squalene_monooxygenase_inhibiti... The selenium dose-response curve has been described as follows: ``The dose response curve of this risk ***essment is much like a U-shaped or inverted U-shaped relationship. The right side of the curve representing the ill effects of deficiency. The approaching trough (or crest in an inverted U-shaped curve) represents the region of adequacy and non-toxicity and finally to the left side of the curve which represents the toxicological dose response.'' ``Is the Current Risk ***essment Paradigm Used by U.S. EPA and Others Compatible with the Concept of Hormesis?
- http://www.belleonline.com/n7v81.html Stress responses make sense to me as extenders of life - since they have the power to activate a broad range of maintenance systems throughout the body.
Invoking selenium's role in anti-oxidant defense as explaining its effect on longevity seems highly unlikely to me by comparison.
The fact that selenium is essential seems to me to be mostly a red herring - the effect is a straightforwards hormetic response - it's just that the gap between selenium activating the body's defenses and it actually causing severe poisoning happens to be wider than is the case of some other toxins (perhaps as a result of adaptations to deal with selenium-rich soils).
Previous study of selenium and hormesis: ``Inorganics and hormesis'' - http://calorierestriction.org/pmid/?n=12809427
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"michaelprice" michaelpr...@ntlworld.com
Hi Tim, I'm a bit rushed, so I'll just quickly respond to a couple of points. More later.: No problem, I've never been keen on making the role of anti-oxidant enzymes central to explaining aging - although many other people try to explain selenium's activity solely in terms of free-radicals, anti-oxidant enzymes etc, I find this unlikely and prefer some sort of deficiency model.
And no doubt plays a role in many other pathways via many other enzymes.
Hmmm... Is there any evidence that selenium is toxic in lower, therapeutically-proven doses?
The simplest explanation is that the LE doses are correcting a (sub-clinical) deficiency. Which doesn't dispute or contradict the evidence for toxicity at higher doses. More evidence (graded experiments) are needed to discriminate between the theories.
Just my immediate thoughts, anyway. I'll read the links you posted this evening. Catch ya' later.
Cheers, Michael C Price
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Tim Tyler t...@tt1lock.org
I paper I found while looking for signs of toxic effects of moderate doses of selenium: ``Adverse health effects of selenium in humans (2001) Epidemiologic studies and case reports have shown that chronic exposure to selenium compounds is ***ociated with several adverse health effects in humans. An early toxic effect of selenium is on endocrine function, particularly on the synthesis of thyroid hormones following dietary exposure of around 300 micrograms Se/d, and on the metabolism of growth hormone and insulin-like growth factor-1.
Other adverse effects of selenium exposure can be the impairment of natural killer cells activity and at higher levels, hepatotoxicity and gastrointestinal disturbances.
Dermatologic effects, such as nail and hair loss and dermatitis, occur after exposure to high levels of environmental selenium. ***essing the toxicity and morbidity after long-term exposure to environmental selenium is difficult: neurotoxicity, particularly the degeneration of motor neurons leading to increased risk of amyotrophic lateral sclerosis, might occur after chronic exposure to both organic and inorganic selenium compounds.
The results of laboratory investigations and cohort studies suggest that selenium species exhibit a bivalent effect in cancer, either increasing or decreasing risk.
Current environmental selenium exposure limits appear to be inadequate for averting adverse health effects.'' - http://calorierestriction.org/pmid/?n=12041880 The figure it gives for "early toxic effect[s]" is less than the one you give as your "Extrapolated Optimal Daily Dose".
By all accounts the "safety margin" with selenium is relatively narrow - the theraputic dose and the toxic one are not that far apart.
I think the way to distinguish between the "hormesis" hypothesis and the "deficiency" hypothesis is probably to either look for signs of stress elsewhere in the organism - or to see how reproductive function is affected by doses of a fair size.
The "deficiency" hypothesis is likely to dominate in populations low in selenium - but the "hormesis" hypothesis may come into play at the doses that life-extensionists are taking.
There seem to be a large number of studies reporting reproductive side effects with selenium - but few can pin themselves down about the dosages involved in their abstracts - and in most cases I expect they are large.
``Effect of selenium-induced oxidative stress on the oxidation reduction system and reproductive ability of male mice.'' - http://calorierestriction.org/pmid/?n=14742902 ...*is* the sort of study I'm thinking of. However they failed to find any negative reproductive side effects of selenium in their "Se-excess" group - so no evidence favouring hormesis there.
Having dug around a bit more, I don't have a great deal of concrete evidence to present which favours the "hormesis" hypothesis over the "deficiency" hypothesis.
I reckon more work is needed on this hypothesis if I expect others to take much notice of it.
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"michaelprice" michaelpr...@ntlworld.com
Hi Tim, Thanks for the info. Do you know whether the 300/d figure relates to both organic and inorganic forms of selenium?
Cheers, Michael C Price
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"michaelprice" michaelpr...@ntlworld.com
Hi Tim, selenomethionine seems to be less toxic, essential and more bioavailable than other forms of selenium: "Se-met metabolism is closely linked to protein turnover. At constant intakes in the nutritional range, tissue Se levels increase until a steady state is established, preventing the build-up to toxic levels." [2] "The ability of SeMet to be incorporated into the body proteins in place of Met furthermore provides a means of reversible Se storage in organs and tissues. This property is not shared by any other naturally occurring selenoamino acid and thus could be ***ociated with a specific physiological function of SeMet. Since higher animals cannot synthesize SeMet, yet from it all needed forms of Se are produced, SeMet meets the criteria of an essential amino acid." [1] "1.5 ppm SeMet in the drinking water. [i.e. human dose equivalent of over 1mg/d - ed] [...] Mice treated with Se showed no signs of toxicity and had significantly less skin damage by UV irradiation" [3] [1] Adv Food Nutr Res. 2003; 47: 73-112.
The nutritional significance, metabolism and toxicology of selenomethionine.
Schrauzer GN.
Biological Trace Element Research Institute, 2400 Boswell Rd., Suite 200, Chula Vista, CA 91914, USA.
SeMet is a naturally occurring toxic amino acid but at the same time represents the major nutritional source of selenium for higher animals and humans. The ability of SeMet to be incorporated into the body proteins in place of Met furthermore provides a means of reversible Se storage in organs and tissues. This property is not shared by any other naturally occurring selenoamino acid and thus could be ***ociated with a specific physiological function of SeMet. Since higher animals cannot synthesize SeMet, yet from it all needed forms of Se are produced, SeMet meets the criteria of an essential amino acid. Accordingly, SeMet, or enriched food sources thereof, are appropriate forms of Se for human nutritional Se supplementation.
However, while SeMet or Se yeast are already widely used in over-the-counter nutritional supplements, infant formulas and parenteral feeding mixtures still contain Se in the form of sodium selenate or sodium selenite, even though these are not the normal nutritional forms of Se. In animal nutrition, these inorganic selenium salts are increasingly replaced by food sources of SeMet such as Se yeast. Synthetic SeMet could also be employed as a feed additive, but its regulatory status is as yet undetermined. The optimal nutritional levels of SeMet for different animal species still need to be determined. The expectation is that lower additions to feedstock of equivalent levels of SeMet will suffice to achieve adequacy than currently approved maximum levels of Se in the form of inorganic Se salts.
Publication Types: Review Review, Tutorial PMID: 14639782 [2] J Nutr. 2000 Jul; 130(7): 1653-6.
Selenomethionine: a review of its nutritional significance, metabolism and toxicity.
Schrauzer GN.
Department of Chemistry and Biochemistry, University of California, San Diego, CA, USA.
Although the need for selenium in human and animal nutrition is well recognized, the question concerning the proper form of selenium for supplemental use is still being debated. Ideally, selenium should be supplemented in the form in which it occurs naturally in foods. Because the L-isomer of selenomethionine (Se-met) is a major natural food-form of selenium, synthetic L-Se-met or enriched food sources thereof such as selenium yeast are appropriate supplemental forms of Se for humans; for animals, DL-Se-met is acceptable. Ingested Se-met is either metabolized directly to reactive forms of selenium or stored in place of methionine in body proteins. Se-met metabolism is closely linked to protein turnover. At constant intakes in the nutritional range, tissue Se levels increase until a steady state is established, preventing the build-up to toxic levels.
Publication Types: Review Review, Tutorial Full-text available PMID: 10867031 [3] Nutr Cancer. 1992; 17(2): 123-37.
The effects of topical and oral L-selenomethionine on pigmentation and skin cancer induced by ultraviolet irradiation.
Burke KE, Combs GF Jr, Gross EG, Bhuyan KC, Abu-Libdeh H.
Department of Pathology, Scripps Clinic and Research Foundation, La Jolla, CA 92037.
This study was conducted to determine whether oral and/or topical selenium (Se) supplementation can reduce the incidence of acute and/or chronic damage to the skin (i.e., sunburn and pigmentation and/or skin cancer, respectively) induced by ultraviolet (UV) irradiation in mice. Groups of 38 BALB:c female mice or 16 Skh:2 hairless pigmented mice were treated with 1) lotion vehicle, 2) 0.02% L-selenomethionine (SeMet) lotion, or 3) vehicle and 1.5 ppm SeMet in the drinking water. Within each group, 30 BALB:c mice or 12 Skh:2 mice were given UV irradiation (Westinghouse FS 40 bulbs) three times per week in doses of 0.575 and 0.24 J/cm2, respectively. The animals' weights and food intakes and the Se concentrations of skin and liver were measured. Skin biopsies were taken from the backs and abdomens of all animals to evaluate the relative amounts of Se and the damage by UV irradiation. Skin pigmentation was scored, and the total number of clinically detectable skin tumors per animal was counted weekly. Results showed that the skin Se concentrations in areas of application of the lotion containing SeMet were greater than those of animals given comparable oral doses, while the Se concentrations of untreated skin and liver were similar to those of animals receiving oral Se. Mice treated with Se showed no signs of toxicity and had significantly less skin damage by UV irradiation, as indicated by reduced inflammation and pigmentation and by later onset and lesser incidence of skin cancer.
PMID: 1584707 Cheers, Michael C Price
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Tim Tyler t...@tt1lock.org
I looked for the study it cited - and found this one - which deals with the effect of 297mcg of Se on thyroid function.
It /looks/ like the study in question - except it was published years later. Anyway: ``Dietary selenium intake modulates thyroid hormone and energy metabolism in men.'' - http://calorierestriction.org/pmid/?n=14608056 It says: ``Decreases of serum T3 and compensatory increases in thyrotropin suggest that a subclinical hypothyroid response was induced in the high selenium group, leading to body weight increases.'' Not very dramatic IMO.
Another study: ``Effects of dietary selenium on sperm motility in healthy men.'' ``[...] The fraction of motile sperm in the high-selenium group decreased by 32% by week 13 and ended 18% lower than baseline. Selenium concentrations changed in seminal plasma but not in sperm, and serum androgen concentrations were unchanged in both groups, indicating this effect was neither androgen dependent nor caused by a change in the selenium supply to the testes. Serum triiodothyronine decreased and thyroid-stimulating hormone increased in the high-selenium group, suggesting that altered thyroid hormone metabolism may have affected sperm motility.
Although this decrease in sperm motility does not necessarily predict decreased fertility, the increasing frequency of selenium supplementation in the healthy population suggests the need for larger studies to more fully ***ess this potential side effect.'' - http://calorierestriction.org/pmid/?n=11545288 This looked at 297 microg/d - and found reproductive side effects.
Double that dose had much more severe side effects in macaques - in: ``two macaques given 600 micrograms Se/kg body weight/day for 10-15 days died'' - http://calorierestriction.org/pmid/?n=1473783 More reproductive side effects - but I'm not sure I can make sense of the doses - as they are expressed as ppm: ``Effects of dietary selenium (SE) on morphology of testis and cauda epididymis in rats.
- http://calorierestriction.org/pmid/?n=10941613 ``Effects of dietary selenium on differentiation, morphology and functions of spermatozoa of the house rat, Rattus rattus L.'' - http://calorierestriction.org/pmid/?n=7519730 These studies are mostly (except the last) by the same researcher.
In some of their abstracts [e.g.
http://calorierestriction.org/pmid/?n=1283694, http://calorierestriction.org/pmid/?n=7801302 http://calorierestriction.org/pmid/?n=1473783] they ...say they are using selenium as L-selenomethionine -
i.e. organic selenium.
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"michaelprice" michaelpr...@ntlworld.com
Hi Tim, as you're probably noticed from another post, I'm focusing now on selenomethionine. I couldn't see anything in the studies you posted that showed toxicity of SeMet, except at huge doses. E.g.: That would be roughly human-equivalent 40 *mg*/d - no wonder some died!
Also magnesium may attenuate Se toxicity: [45] Effect of dietary selenium and magnesium on human mammary tumor growth in athymic nude mice. Yan L, Boylan LM, Spallholz JE in Nutr Cancer 1991;16(3-4):239-48 PMID: 1775386 "Low dietary Mg also resulted in an apparent increase in Se toxicity in these animals." Cheers, Michael C Price
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Tim Tyler t...@tt1lock.org
Yes sorry - I didn't notice the (important) "per kg" here ;-) The doses in the first two studies: ``Dietary selenium intake modulates thyroid hormone and energy metabolism in men.'' - http://calorierestriction.org/pmid/?n=14608056 ``Effects of dietary selenium on sperm motility in healthy men.'' - http://calorierestriction.org/pmid/?n=11545288 ...both dealt with absolute doses of 297 mcg per day in men.
Both studies say: ``Eleven healthy men were fed a controlled diet of foods naturally high or low in selenium for 120 days while confined in a metabolic research unit.'' I believe that effectively means that they used L-selenomethionine.
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"michaelprice" michaelpr...@ntlworld.com
Tim Tyler wrote or quoted: Hmmm. Interesting result. You're probably right, but I'd like to see the form of dietary selenium specified.in black and white, since it is so important.
Cheers, Michael C Price
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